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Lp(a) Lipoprotein/pre‐β 1 ‐lipoprotein, serum lipids and atherosclerotic disease
Author(s) -
DAHLEN G.,
BERG K.,
FRICK M. H.
Publication year - 1976
Publication title -
clinical genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 102
eISSN - 1399-0004
pISSN - 0009-9163
DOI - 10.1111/j.1399-0004.1976.tb01613.x
Subject(s) - lipoprotein(a) , lipoprotein , medicine , triglyceride , population , cholesterol , endocrinology , blood lipids , environmental health
With appropriate electrophoretic techniques and fresh serum samples, the Lp(a) lipo‐protein/pre‐β 1 ‐lipoprotein is demonstrable as a distinct zone in the area between β 1 ‐lipo‐protein and ordinary pre‐β 1 ‐lipoprotein, when sera which are strongly positive with respect to the Lp(a) antigen are analyzed. The Lp(a) lipoprotein is a genetically determined normal serum component. The phenotype Lp(a+) was found significantly more frequently in two series of patients with coronary heart disease (CHD) than in appropriate controls. The frequency difference between patients and controls was particularly pronounced for the Finnish samples studied, 55 % of the patients having the phenotype Lp(a +), as opposed to only 31 % of the healthy controls. As judged from electrophoresis strips, high concentrations of Lp(a) lipo‐protein/pre‐β 1 ‐lipoprotein were positively correlated with coronary score as determined by angiography. This correlation was highly significant. Total serum cholesterol value was slightly higher in Lp(a +) than in Lp(a‐) persons from two of the four population samples studied, but no statistically significant difference was found. Serum triglyceride levels exhibited a statistically insignificant trend towards higher values in Lp(a‐) than in Lp(a+) individuals, in three of the four samples tested. The strong association between the phenotype Lp(a+) and CHD, as well as the correlation between high amounts of Lp(a) lipoprotein/pre‐β 1 ‐lipoprotein and coronary score on one hand, and the weak correlation between presence of Lp(a) lipoprotein/pre‐β 1 ‐lipoprotein and lipid values on the other, make it highly unlikely that the increased frequency of the Lp(a+) phenotype in CHD patients merely reflects an over‐all increase of the intravascular pool of LDL and/or VLDL reflected in increased serum levels of cholesterol and/or triglycerides. By the same token, it is unlikely that the insignificant effect on lipid values can, on its own, explain the correlation between Lp(a) phenotype and CHD.